NAD+

β-Nicotinamide adenine dinucleotide

The cellular coenzyme at the center of the metabolism-and-aging conversation

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme present in every living cell. It shuttles electrons in the redox reactions that power energy metabolism, and it is the required substrate for sirtuins and PARP enzymes involved in DNA-repair and stress-response signaling. Tissue NAD+ levels fall with age, which is why it sits at the center of longevity research — though most of the rigorous human data is on NAD+ precursors, not NAD+ dosed directly.

Class
Dinucleotide coenzyme (not a peptide)
Origin
Endogenous — synthesized in all living cells
Evidence stage
Human trials — largely on precursors (NR/NMN)
Research focus
Energy metabolism · sirtuins · DNA repair

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What the Research Actually Says

Every claim below is cited to the published literature and labeled by how far the evidence has actually progressed. Numbers refer to the reference list at the bottom of the page.

NAD+ decline, metabolism & aging

Preclinical (cell & animal)

A large body of cell and animal work ties falling NAD+ levels to features of aging and metabolic dysfunction, with restoration of NAD+ improving mitochondrial and metabolic markers in model systems. This is the framework behind most NAD+ interest, summarized in widely-cited reviews.

References: [1] [2]

Energy homeostasis & mitochondrial function

Preclinical (cell & animal)

NAD+ availability governs the balance of energy metabolism between the mitochondria and the nucleus, acting as both a redox carrier and a signaling cofactor. Much of the mechanistic detail comes from cell and rodent models.

References: [2]

Boosting NAD+ in humans (precursor trials)

Early human trials

Human trials of NAD+ precursors — nicotinamide riboside (NR) and NMN — show they are generally well tolerated and can raise blood NAD+ markers. Important nuance: these studies test precursors, not NAD+ administered directly, and clinical endpoints beyond biomarker changes remain limited.

References: [3] [4]

Where the Evidence Stops

  • ◆The strongest human data is on NAD+ precursors (nicotinamide riboside, NMN), not on NAD+ given directly. Extrapolating precursor results to direct NAD+ is an assumption, not a finding.
  • ◆Whether directly administered NAD+ meaningfully raises intracellular NAD+ — rather than being broken down first — is still debated.
  • ◆Injectable and IV NAD+ are offered in some wellness clinics, but controlled trial support for those protocols is thin.
  • ◆NAD+ is a coenzyme, not a peptide; it is grouped here as a research compound, not a peptide therapeutic.
Sourcing NAD+

Research-grade NAD+, batch-documented

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Sold for laboratory research use only — not for human consumption.

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References

  1. Verdin E NAD+ in aging, metabolism, and neurodegeneration. Science, 2015.
  2. Cantó C, Menzies KJ, Auwerx J NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus. Cell Metabolism, 2015.
  3. Martens CR, et al. Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+ in healthy middle-aged and older adults. Nature Communications, 2018.
  4. Rajman L, Chwalek K, Sinclair DA Therapeutic potential of NAD-boosting molecules: the in vivo evidence. Cell Metabolism, 2018.

More compound profiles

Published 2026-08-25. Reviewed against the cited primary literature.

This page is for educational purposes only and is not medical advice. Peptides discussed here are research compounds; nothing here is a recommendation to use them. Consult a qualified healthcare provider about anything affecting your health.

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